Experimental studies of electroacupuncture on ventricular fibrillation threshold in rats with acute ischemic myocardium

Summary By ligating the proximate left anterior descend (LAD) of coronary artery and inducing the ventricular fibrillation with electrical stimulation, the preventive effects of electroacupuncture (EA) on ventricular fibrillation were observed. The results showed that the ventricular fibrillation threshold (VFT) of rats with acute ischemic myocardium was raised after acupuncturing some acupoints, which could prevent the occurrence of ventricular fibrillation. Furthermore, the combination of EA and propranolol could enhance the VFT effectively, and they showed a good synergistic effect. This project was supported by grants from National Natural Science Foundation of China (No. 3870563).     

The role of Na+/K+ ATPase activity during low flow ischemia in preventing myocardial injury: A 31P, 23Na and 87Rb NMR spectroscopic study

An increase in intracellular Na⁺ during ischaemia has been associated with myocardial injury. In this study, we determined whether inhibition of Na⁺/K⁺ ATPase activity contributes to this increase and whether Na⁺/K⁺ ATPase activity can be maintained by provision of glucose to perfused rat hearts during low flow, 0.5 ml/min, ischemia. We used ³¹P NMR spectroscopy to determine changes in myocardial energetics and intracellular and extracellular volumes. ²³Na NMR spectroscopy, with DyTTHA^3- present as a shift reagent, was used to measure changes in intracellular Na⁺ and ⁸⁷Rb NMR spectroscopy was used to estimate Na⁺/K⁺ ATPase activity from Rb⁺ influx rates, Rb⁺ being an NMR-sensitive congener of K⁺. In hearts provided with 11 mM glucose throughout ischemia, glycolysis continued and ATP was twofold higher than in hearts without glucose. In the glucose-hearts, Rb⁺ influx rate was threefold higher, intracellular Na⁺ was fivefold lower at the end of ischemia and functional recovery during reperfusion was twofold higher. We propose that continuation of glycolysis throughout low flow ischemia allowed maintenance of sufficient Na⁺/K⁺ ATPase activity to prevent the increase in intracellular Na⁺ that would otherwise have led to myocardial injury.     

鼠脑缺血后软脑膜微循环及脑血流自动调节功能的实验研究

本文利用闭合式颅骨开窗的方法制成脑微循环小室,以显微镜摄像系统连续观察双侧颈总动脉阻塞前后软脑膜微循环的变化,发现双侧颈总动脉阻塞后,软脑膜动脉管径和平均动脉压分别增加了40％和58％;静脉内血球流速减少至原值的70％;软脑膜动脉对动脉血二氧化碳浓度升高及低血压所引起的扩张反应受到明显抑制。实验结果提示:双侧颈总动脉阻塞后,虽然脑动脉明显扩张、血压上升。仍不足以代偿由于脑局部灌注压的下降所造成的脑血流量减少。提示双侧颈总动脉阻塞时,脑血流的自动调节功能受到严重损害。     

颅脑超声对高原新生儿缺氧缺血性脑病观察及探讨

本文对西宁地区新生儿缺氧缺血性脑病（ＨＩＥ）颅脑超声诊断分析脑缺氧缺血产生的原因、脑实质损伤程度及预后评估。提出对围产期窒息导致脑缺血性损害的预防措施。     

Comparative effects of ischemia and acute hypoxemia on muscle afferents from tibialis anterior in cats

Comparative effects of ischemia and acute hypoxemia (PaO₂ = 24 mm Hg) were studied in anesthetized cats on afferents from the tibialis anterior limb muscle. Metaboreceptors (groups III and IV fibers) and mechanoreceptors were identified by their activation by an intraarterial injection of lactic acid (LA) or high-frequency vibrations (HFV) applied to the extremity of the muscle tendon, respectively. Ischemia and hypoxemia exerted opposite influences on the two categories of muscle afferents: they depressed the response of mechanoreceptors to HFV, but markedly enhanced the spontaneous tonic activity of metaboreceptors. The effects of hypoxamia were delayed but slightly greater and lasted longer during the recovery period than those exerted by ischemia. The inhibitory action on mechanoreceptors exerted by a reduced oxyden supply to muscle is interpreted as a result from local acidosis. Indeed, under normoxic conditions, a LA bolus injection during the HFV test also reduced the firing rate of these receptors. © 1993 John Wiley & Sons, Inc.     

“强力”饮料对大鼠心肌组织化学的影响

“强力”饮料是增强体质的强壮饮料,内含多种氨基酸、微量元素和维生素。临床观察和动物试验已证明可改善人和动物的运动能力。30支Wistar雄性大鼠随机地分为三组:实验Ⅰ组、实验Ⅱ组和对照组。实验Ⅰ组每日服“强力”饮料,实验Ⅱ组每日服水。观察10天后,实验组Ⅰ和Ⅱ配对进行最大游泳试验。左心肌进行了下述组化反应:糖原:Akpase,ACPase ATPase和SDH。结果说明实验Ⅰ组和Ⅱ组的糖原,AKPase和ACPase之间存在明显的差异。结论为强力饮料可能改善或延缓大鼠运动时心肌缺血。     

The effect of human SOD on the survival rate in rats with temporary splanchnic ischemia

The accumulation of oxygen free radicals is reported to occur in the organs subjected to temporary ischemia followed by reperfusion, resulting in the fatal outcome of the animals. The effects of human SOD, a representative scavenger of oxygen free radicals, on the survival rates were investigated in the rats with temporary splanchnic ischemia. The temporary ischemia was induced by the occlusion of anterior mesenteric and celiac arteries for 30min under anesthesia. Prior and after treatment with 2mg/100g of human SOD, iv or sc, produced significant improvements in survival rates. Human SOD, cloned from human placenta DNA and expressed in microorganisms, has extreme homogeneity. The results suggest the possible introduction of human SOD into clinical field as an effective scavenger of oxygen free radicals.(Ogawa R, Bitoh H, Ohi Y: The effect of human SOD on the survival rate in rats with temporary splanchnic ischemia. J Anesth 2: 41–45, 1988)     

自身免疫性溶血性贫血20例临床分析

本文报道温抗体型自身免疫性溶血性贫血20例,其中包括特殊类型“兼有冷抗体和温抗体的自身免疫性溶血性贫血”3例,伴有血小板减少性紫瘢的Fisher—Evans综合征4例。并对本病致病因素、发病年龄、临床表现及特殊类型产生机理进行了讨论。     

TCD结合TCCD与DSA对脑动脉狭窄的一致性分析及对治疗方案的指导价值

目的 探究经颅多普勒超声(transcranial Doppler sonography, TCD)结合经颅彩色多普勒超声(transcranial color-coded duplex, TCCD)与数字减影血管造影(digital subtraction angiography, DSA)对脑动脉狭窄的一致性分析及对治疗方案的指导价值。方法 选取缺血性脑血管病患者100例,均行TCD、TCCD及DSA检查,以DSA检查结果作为“金标准”,分析脑动脉狭窄程度,观察不同狭窄程度患者TCD、TCCD超声表现,采用Kappa检验分析TCD结合TCCD诊断脑动脉狭窄程度与DSA检查结果的一致性,比较不同狭窄程度患者收缩期峰流速(systolic velocity, Vs)、平均峰流速(mean velocity, Vm)、搏动指数(pulsatility index, PI),采用Spearman相关系数模型分析Vm、PI与脑动脉狭窄程度的相关性,所有患者均行药物或手术治疗,比较不同治疗方法患者入院时、治疗后6个月Vs、Vm、PI。结果 100例缺血性脑血管病患者,轻度狭窄42例,中度狭窄3...     

Antiarrhythmic actions of tedisamil: Studies in rats and primates

Tedisamil is a new bradycardic agent, previously shown to block transient outward and delayed rectifier potassium currents in cardiac tissue [1,2]. In the present study tedisamil caused bradycardia and Q-Tc widening in rats and primates. Q-Tc widening is indicative of class III antiarrhythmic actions. In keeping with this, tedisamil had antiarrhythmic activity against electrical and ischemia-induced arrhythmias in rats. In rats, 0.5–4 mg/kg IV tedisamil caused parallel and dose-related increases in action-potential duration, Q-Tc interval, and refractory period; and decreases in maximum ventricular following frequency. In primates after 0.5–2.0 mg/kg IV, findings were similar for indices of Q-T widening and decreases in maximum ventricular following frequency. Tedisamil did not change QRS width, nor did it increase threshold currents for capture of ventricles, nor for fibrillo-flutter at doses below 4 mg/kg in rats. These findings were consistent with the lack of significant sodium-channel blockade. However, upon increasing the dose to 4 mg/kg, ventricular fibrillo-flutter could not be induced in rats by electrical stimulation; instead, only ventricular tachycardias with slow rates occurred. Ischemia-induced ventricular fibrillation was reduced in a dose-related manner by tedisamil in rats. The overall incidence of ischemia-induced ventricular tachycardia was not markedly reduced, but rates during tachycardic episodes were lower. When pacing was used to overcome tedisamil-induced bradycardia, antiarrhythmic actions during ischemia were more pronounced. These findings are consistent with the hypothesis that tedisamil increased refractoriness, which resulted in extended path lengths for reentry circuits and slower rates during episodes of ventricular tachycardia. High doses of tedisamil increased path lengths so much that the multiple reentry circuits of fibrillation could no longer occur. The limited study in primates suggests similar mechanisms could occur in humans.